Lifting weights during chemo raised IL-17 by 76% in women with breast cancer

Key Findings

🧬 A Worm Protein Links Mitochondrial Stress to Longer Life — and It Has a Human Cousin

• In C. elegans (a tiny worm used in aging research), a forward genetic screen identified FUBL-3 — the worm version of human FUBP1 — as a protein that moves into cell nuclei when mitochondria are under stress
• Worms missing FUBL-3 lost the ability to compact their chromatin (DNA packaging) under stress and gained no extra lifespan from mitochondrial stress; worms with extra FUBL-3 showed chromatin restructuring and lived longer
• Human FUBP1 rescued the worm mutants and also triggered chromatin remodeling in mammalian cells under mitochondrial stress, suggesting the mechanism is conserved across species

This worm-to-mammal conservation suggests FUBP1 may be worth investigating as part of how cells communicate mitochondrial distress to the nucleus during aging — though whether this translates to human lifespan is unknown.

💊 A Network Medicine Approach Mapped 2,358 Longevity Genes to Find Drug Repurposing Candidates

• Researchers mapped 2,358 longevity-associated genes onto a human protein interaction network and measured how close 6,442 existing drug compounds sit to each of aging's hallmarks (like inflammation, genomic instability, etc.)
• They then added a second metric — pAGE — that checks whether a drug's known gene expression effects push cells toward or away from known age-related expression patterns within each hallmark
• Combining network proximity + pAGE produced ranked drug-repurposing candidates for specific aging hallmarks, with interpretable molecular mechanisms for why each candidate might work

This framework, published in Nature Aging, could help prioritize which existing approved drugs are worth testing in longevity trials — though the candidates still require experimental and clinical validation.

🧠 Psychosis Linked to ~0.56 Years of Extra Metabolic Aging in 225,000 UK Biobank Participants

• Among 225,212 UK Biobank participants, those with a psychosis diagnosis had a metabolite-predicted age that was ~0.56 years older than their chronological age (95% CI: 0.25–0.86)
• Substance use, affective, and neurotic disorders were also linked to older metabolomic age, while obsessive-compulsive and eating disorders were associated with a younger metabolomic age than expected
• Interestingly, polygenic scores (genetic liability) for psychosis and tobacco use disorder predicted a younger metabolomic age, diverging from the clinical pattern — suggesting non-genetic factors drive much of the biological aging difference

Biological aging doesn't move in one direction uniformly across mental health conditions — and the gap between genetic risk and clinical phenotype suggests environment and behavior play a large role.

🫀 A Kidney Enzyme Called mPGES-2 May Drive Both Renal Aging and Bone Loss in Mice

• In aged mice, genetic deletion of Ptges2 (the gene encoding mPGES-2, an enzyme in kidney podocytes) improved health indices, prolonged median survival, and reduced glomerulosclerosis (kidney scarring) and kidney senescence
• Single-cell analysis showed podocyte mPGES-2 — not tubular mPGES-2 — was the dominant driver; its mechanism appears to involve PGE/EP1 signaling that pushes podocytes into a senescent state
• Podocyte-specific deletion also reduced age-related osteoporosis and restored levels of calcitriol and α-klotho (kidney hormones that influence bone), suggesting a kidney-to-bone signaling link; a drug inhibitor (SZ0232) replicated these effects with no apparent toxicity in major organs

In mice, blocking this kidney enzyme appears to slow both renal aging and bone loss simultaneously — a potential two-for-one target worth watching, though human relevance remains to be tested.

🧫 Senescent and Reactive Brain Cells Look Similar But Behave Differently

• Using a strictly controlled lab model in human astrocytes (support cells of the brain), researchers compared senescent astrocytes (permanently arrested cells) vs. reactive astrocytes (stress-activated cells) using gene expression profiling
• Reactive astrocytes predominantly expressed genes tied to inflammation; senescent astrocytes expressed a secretory profile suggesting involvement in synaptic pruning (trimming of brain connections)
• In a neurite outgrowth test, senescent astrocytes still supported nerve fiber growth, while reactive astrocytes lost that capacity — an unexpected functional divergence

This preprint-stage work suggests that treating all "stressed" brain cells as equivalent may miss meaningful biological differences — and that existing tools for detecting senescent cells may not cleanly separate these two states.

📊 A Lipidomic 'Metabolic Age Score' Adjusted for Lifestyle Predicted Alzheimer's and Heart Disease Across ~20,000 People

• Researchers built a plasma lipid-based biological age model (EAmAge) that first statistically removes major environmental influences (diet, lifestyle) before estimating age — designed to capture more "intrinsic" metabolic aging
• Validated across four cohorts totaling ~20,174 people (AusDiab: n=10,339; BHS, ADNI, ASPREE: n=9,835), EAmAge showed stronger and more consistent associations with incident Alzheimer's-related dementia, cardiovascular events, and all-cause mortality than an unadjusted lipid age model
• EAmAge also correlated with Alzheimer's biomarkers including amyloid burden, reduced brain glucose metabolism, and hippocampal shrinkage

This preprint-stage score may offer a way to track biological aging that's less confounded by day-to-day lifestyle choices — potentially useful for separating who is aging faster at a biological level from who simply has an unhealthy diet.